RESUMO
We describe a case of erythema induratum of Bazin (EIB) that presented recurrently on the extremities during treatment with anti-tuberculosis medications. The anti-tuberculosis medications were effective, so they were continued despite the occurrence of the EIB lesions, and those lesions disappeared 5 months after first appearing. EIB is currently considered a multifactorial disorder with many different causes, with tuberculosis being an example, and it is thought to be a hypersensitive immune response to Mycobacterium tuberculosis. The clinical manifestations may fluctuate depending on the immune response of the host. Our patient was affected with myelodysplastic syndrome, and we believe that this was a major factor that interfered with a normal immune response. This case illustrates the importance of providing intensive anti-tuberculosis treatment from the start, and in cases where EIB co-presents, to continue this treatment until the end, in order to prevent relapse.
Assuntos
Antituberculosos , Eritema Endurado , Síndromes Mielodisplásicas , Humanos , Síndromes Mielodisplásicas/complicações , Síndromes Mielodisplásicas/tratamento farmacológico , Eritema Endurado/tratamento farmacológico , Eritema Endurado/patologia , Antituberculosos/uso terapêutico , Recidiva , Masculino , Idoso , FemininoRESUMO
A Japanese male in his 30s with no underlying medical condition presented with painless nodules after being bitten by a dog during a stay in Bali, Indonesia, 7 years earlier. He was referred to our department with multiple ulcers, nodules, and masses on the right leg. The final diagnosis was mycetoma caused by Nocardia vulneris, which may have been exacerbated by colonization of Candida parapsilosis and C. tropicalis as these yeasts were isolated by culture from the tissue. Treatment with minocycline hydrochloride and sulfamethoxazole trimethoprim showed partial efficacy, but the addition of posaconazole achieved significant efficacy. This suggests that the surmised coexistence of pathogenic yeasts of lower virulency may have made mycetoma in this case intractable.
RESUMO
Leprosy, a chronic infectious disease caused by Mycobacterium leprae, was identified by G. H. A. Hansen in 1873. The different clinical presentations of the disease are determined by the quality of the host immune response. The bacteria have affinity for the peripheral nerves and are likely the cause of neuropathy, a cardinal manifestation of the disease. WHO recommends a protocol of multidrug therapy (MDT), which effectively controls the disease, hence contributing to the global elimination program. Early detection of leprosy and treatment by MDT are the most important steps in preventing deformity and disability.
Assuntos
Humanos , Comorbidade , Esquema de Medicação , Farmacorresistência Bacteriana , Hansenostáticos/efeitos adversos , Hansenostáticos/uso terapêutico , Hanseníase/classificação , Hanseníase/diagnóstico , Hanseníase/epidemiologia , Hanseníase/tratamento farmacológico , Países em Desenvolvimento , Quimioterapia Combinada , PrevalênciaRESUMO
The antigenicity of Mycobacterium leprae (M. leprae)-derived cell membrane fraction was examined using human dendritic cells (DCs). Immature DCs internalized and processed the cell membrane components, and expressed M. leprae-derived antigens (Ags) on their surface. The expression of MHC class II, CD86, and CD83 Ags on DCs and CD40 ligand (L)-associated IL-12 p70 production from DCs were up-regulated by the membrane Ags. Moreover these stimulated DCs induced significantly higher level of interferon-gamma (IFN-gamma) production by autologous CD4(+) and CD8(+) T cells than those pulsed with equivalent doses of live M. leprae or its cytosol fraction. Both subsets of T cells from tuberculoid leprosy patients also produced several fold more IFN-gamma than those from normal individuals. Furthermore, the intracellular perforin production in CD8(+) T cells was up-regulated in an Ag-dose dependent manner. These results suggest that M. leprae membrane Ags might be useful as the vaccinating agents against leprosy.